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Cyclic AMP decreases the availability of 5-phosphoribosyl-1-pyrophosphate and decelerates de novo purine synthesis in rat hepatocytes.

机译:环状AMP降低了大鼠肝细胞中5-磷酸核糖基-1-焦磷酸的利用率,并降低了嘌呤从头合成的速度。

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摘要

Cyclic adenosine monophosphate (cAMP) was found to decrease the availability of 5-phosphoribosyl-1-pyrophosphate (PRPP) and to decelerate the rate of de novo purine synthesis in suspensions of adult rat hepatocytes. Glucagon did not affect these parameters. The glucagon antagonist des-His1[Glu9]glucagon amide (DHGA), and the protein kinase C activator 1,2-dioctanoyl-sn-glycerol (DOG) were also found to lower PRPP availability. Incubation of the hepatocytes with dbcAMP or with DHGA, did not alter the activity of PRPP synthetase in the hepatocyte lysates, indicating that the above effects are not mediated through the activity of this enzyme. The possibility that the decrease in PRPP availability reflects increased consumption associated with accelerated pyrimidine synthesis is discussed. The decelerated rate of de novo purine synthesis is probably secondary to the decreased PRPP availability.
机译:发现环状腺苷一磷酸(cAMP)降低了成年大鼠肝细胞悬液中5-磷酸核糖基-1-焦磷酸(PRPP)的利用率,并降低了嘌呤从头合成的速率。胰高血糖素不影响这些参数。还发现胰高血糖素拮抗剂des-His1 [Glu9]胰高血糖素酰胺(DHGA)和蛋白激酶C激活剂1,2-二辛酰基-sn-甘油(DOG)降低了PRPP的利用率。用dbcAMP或DHGA孵育肝细胞不会改变肝细胞裂解液中PRPP合成酶的活性,表明上述作用不是通过该酶的活性介导的。讨论了PRPP可用性下降反映了与嘧啶合成加速相关的消耗增加的可能性。从头嘌呤合成的速率降低可能是PRPP可用性降低的原因。

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